• Gastric cancer is the 5th most common cancer worldwide and the 4th leading cause of cancer death globally (2022 GLOBOCAN data).
• There is a declining overall incidence trend globally — attributed to declining H. pylori prevalence (improved sanitation, eradication therapy), better food preservation (refrigeration replacing smoking/salting/pickling), and reduced smoking rates ^[1][2].
• However, there is an increasing trend of proximal/cardia gastric cancer in Western countries — thought to be related to rising obesity and gastro-oesophageal reflux disease (GORD) ^[2].
• Incidence: decreasing trend (6th incidence, 4th mortality), but increased in Asia (Japan: diet-related) ^[2].
• Geographic variation is striking: highest incidence in East Asia (Japan, South Korea, China), parts of South America, and Eastern Europe; lowest in North America, Northern Europe, and Africa.
  • Why East Asia? High prevalence of H. pylori, dietary factors (pickled vegetables, high-salt diet, smoked fish), and possibly genetic susceptibility.
  • Japan and South Korea have national screening programmes (endoscopy-based) → detect more early gastric cancers → better survival statistics.

• M:F ratio ≈ 1.5:1 ^[3]
• Incidence rate in HK (most recent Hong Kong Cancer Registry data):
  • Overall: 6th most common cancer ^[2][3]
  • Male: 5th most common cancer
  • Female: 9th most common cancer
• Mortality rate in HK:
  • Male: 5th most common cause of cancer death
  • Female: 5th most common cause of cancer death ^[3]

^[2]

• Cell type: adenocarcinoma (90%) > lymphoma (5%) > GIST, metastasis ^[2]
• Site: distal stomach (antrum/pylorus) > cardia (increasing trend) > OGJ ^[2]

The stomach is a J-shaped muscular organ divided into:

1. Cardia — the region immediately surrounding the gastro-oesophageal junction (GOJ); narrow zone where oesophageal squamous epithelium transitions to gastric columnar epithelium.
2. Fundus — the dome-shaped portion superior and lateral to the cardia, sitting against the left hemidiaphragm; acts as a gas reservoir.
3. Body (corpus) — the largest region; contains the majority of parietal cells (HCl production) and chief cells (pepsinogen production).
4. Antrum — the distal "prepyloric" portion; rich in G cells that secrete gastrin, which stimulates parietal cells.
5. Pylorus — the sphincteric muscle controlling gastric emptying into the duodenum.

The lesser curvature (medial, shorter) and greater curvature (lateral, longer) are the two borders. The angular incisure (incisura angularis) is the notch on the lesser curvature that marks the transition from body to antrum — a common site for Type I gastric ulcers and also a common biopsy site for surveillance.

All derived from the coeliac trunk (axis):

Lesser curvature:

• Left gastric artery — directly from the coeliac trunk (largest contributor to gastric blood supply)
• Right gastric artery — from the common hepatic artery (or proper hepatic artery)

Greater curvature:

• Short gastric arteries — from the splenic artery (supply the fundus)
• Left gastro-omental (gastroepiploic) artery — from the splenic artery
• Right gastro-omental (gastroepiploic) artery — from the gastroduodenal artery

^[3][4]

This rich anastomotic network means the stomach has excellent blood supply and can survive ligation of most of its arterial branches, which is why partial gastrectomy is feasible. However, the rich vascularity also means gastric tumours can bleed significantly.

Venous drainage mirrors the arterial supply and ultimately drains into the portal venous system → this explains why the liver is the most common site of haematogenous metastasis from gastric cancer.

• Left and right gastric veins → portal vein
• Short gastric veins and left gastro-omental vein → splenic vein
• Right gastro-omental vein → superior mesenteric vein

Gastric lymph nodes are classified into 16 stations (Japanese Gastric Cancer Association classification), grouped into tiers:

• N1 (perigastric): Stations 1–6 — along the lesser and greater curvatures
• N2 (regional): Stations 7–11 — along the named arteries (left gastric, common hepatic, coeliac, splenic artery, splenic hilum)
• N3 (distant): Stations 12–16 — para-aortic, retropancreatic, mesenteric root

The extent of lymphadenectomy during gastrectomy (D1 vs D2 vs D3) is defined by how many of these tiers are removed. D2 lymphadenectomy (removing N1 + N2 stations) is the standard of care in East Asia (including HK) for curative-intent surgery.

• Sympathetic: Greater splanchnic nerve (T5–T9 sympathetic trunk) → coeliac ganglion → postganglionic fibres ^[4]
• Parasympathetic:
  • Anterior vagal nerve (primarily from the left vagus): supplies the stomach, pylorus, and liver ^[4]
  • Posterior vagal nerve (primarily from the right vagus): supplies the stomach and the foregut/midgut down to the splenic flexure ^[4]

The vagus nerve is critical because it stimulates gastric acid secretion (via direct acetylcholine on parietal cells and indirectly via gastrin release). This is why vagotomy was historically used for peptic ulcer disease. In gastric cancer surgery, the vagal trunks are inevitably divided during gastrectomy, contributing to post-operative dumping syndrome and altered gastric motility.

1. Mucosa (epithelium + lamina propria + muscularis mucosae)
2. Submucosa — contains Meissner's plexus, rich lymphatic and blood vessels
3. Muscularis propria — inner oblique, middle circular, outer longitudinal; contains Auerbach's (myenteric) plexus
4. Serosa (visceral peritoneum) — covers most of the stomach except the bare area posteriorly

The T-staging of gastric cancer is based on depth of invasion through these layers, which is why understanding them is essential.

• Previous partial gastrectomy (> 20 years) ^[1]
• Allows reflux of bile causing chronic gastritis → reactive/chemical gastropathy → atrophy → metaplasia → carcinoma ^[3]
• Typically occurs at the gastric remnant, especially at the gastrojejunal anastomosis (stump carcinoma)
• Risk increases ≥15–20 years post-surgery
• Billroth II reconstruction carries higher risk than Billroth I (because of greater bile reflux)

Harmful dietary factors: ^[1]

• N-nitroso compounds — powerful carcinogens; formed from dietary nitrates/nitrites by bacterial conversion (especially in hypochlorhydric stomachs where bacteria colonise)
• Preserved, smoked, salted food — high in nitrates, nitrosamines, and salt, which damages gastric mucosa directly and promotes H. pylori colonisation
• Pickled food ^[3] — common in East Asian diets, contributing to the high incidence in this region

Protective dietary factors: ^[1]

• Trace elements (e.g. selenium) — antioxidant (selenoproteins like glutathione peroxidase neutralise reactive oxygen species)
• Vitamin C — antioxidant that also inhibits the formation of N-nitroso compounds in the stomach
• Fresh fruits and vegetables — source of antioxidants and fibre

Industrial/occupational exposures: ^[1]

• Dusty, high temperature, rubber, coal mining, metal processing, chromium production — occupational carcinogen exposure

• Smoking (11% attributable risk) ^[1] — nitrosamines in tobacco smoke; also impairs gastric mucosal defence
• Alcohol — damages gastric mucosa directly; may have synergistic effect with H. pylori and smoking ^[3]
• Obesity — particularly associated with cardia/GOJ gastric cancer; mechanism: increased intra-abdominal pressure → GORD → Barrett's → proximal cancer; also chronic low-grade inflammation, hyperinsulinaemia ^[3]
• Low socioeconomic status ^[3] — correlates with higher H. pylori prevalence, poorer diet, and limited access to healthcare

• Primary immunodeficiency → chronic gastric infection/inflammation → atrophic gastritis → increased gastric cancer risk
• Also associated with gastric lymphoma

This is the classic multi-step model proposed by Pelayo Correa:

Why does this sequence happen?

• Chronic mucosal injury → repeated cycles of cell death and regeneration → increased cell turnover → greater chance of DNA replication errors
• Achlorhydria (from parietal cell loss) → bacterial overgrowth → increased nitrosamine production in the stomach
• Hypergastrinaemia (compensatory, from loss of acid feedback) → trophic effect on mucosal cells → promotes proliferation
• Accumulation of genetic mutations (TP53, APC, KRAS, microsatellite instability) drives progression through each stage

• Does not follow the Correa cascade
• Driven by loss of E-cadherin (CDH1 mutation — germline in HDGC, or somatic/epigenetic silencing in sporadic cases)
• E-cadherin loss → disrupted cell-cell adhesion → individual tumour cells infiltrate diffusely through the gastric wall (no glandular formation)
• Characterised by signet ring cells — tumour cells with large intracytoplasmic mucin vacuoles that push the nucleus to the periphery, giving a "signet ring" appearance
• More likely to invade transmurally and seed the peritoneum early

Modern molecular classification divides gastric cancer into 4 subtypes:

Gastric cancer spreads by four routes:

1. Direct invasion — into adjacent organs (pancreas, transverse colon, spleen, liver, diaphragm)
2. Lymphatic spread — to perigastric, coeliac, para-aortic lymph nodes; most common route
3. Haematogenous spread — via portal vein to liver (most common distant metastatic site); also lung, bone, brain (uncommon) ^[3]
4. Transcoelomic (peritoneal) spread — once the tumour penetrates the serosa (T4a), cancer cells shed into the peritoneal cavity → peritoneal carcinomatosis, malignant ascites, Krukenberg tumour (bilateral ovarian metastases — signet ring cells implanting on the ovaries)

Spread to: liver / peritoneum / lymph nodes (common); brain / lung / ovary / bone (uncommon) ^[3]

This is the most clinically useful histological classification:

^[2]

Classifies the gross appearance of advanced gastric cancer:

• Aggressive form of poorly-differentiated diffuse-type gastric cancer
• Broad region of gastric wall is extensively infiltrated by malignancy resulting in a rigid, thickened stomach termed linitis plastica ("leather bottle" stomach)
  • "Linitis" = from Latin linum (linen/flax); "plastica" = moulded — the stomach becomes stiff like starched linen
• Difficult to diagnose with upper endoscopy; barium swallow is superior ^[3]
  • Tumours tend to infiltrate the submucosa and muscularis propria and therefore superficial mucosal biopsy can be false-negative ^[3]
  • Combination of strip and bite biopsy technique should be used when there is suspicion of a diffuse-type gastric cancer ^[3]
• Poor prognosis: ^[3]
  • Late presentation with advanced stage at diagnosis
  • Potential for early spread with 1/3 of patients having metastatic disease to peritoneum (malignant ascites) at diagnosis
  • Presence of microscopic disease at surgical margins due to its diffuse nature

Note: "Early" here is a pathological definition referring to depth of invasion — NOT size or symptoms. An early gastric cancer can be quite large but still confined to the mucosa/submucosa.

T (Primary Tumour):

N (Regional Lymph Nodes):

A minimum of 16 lymph nodes must be examined for adequate staging (this is why D2 lymphadenectomy is preferred).

M (Distant Metastasis):

• M0: No distant metastasis
• M1: Distant metastasis (including positive peritoneal cytology)

This is the most common presentation of gastric cancer, but dyspepsia affects ~25% of the population and is overwhelmingly benign ^[8].

Gastric cancer accounts for a small proportion of UGIB — peptic ulcer disease is by far the most common cause ^[8][11].

GOO is malignant until proven otherwise — 80% malignant, 20% benign ^[2][12].

When gastric cancer involves the cardia or GOJ, the presentation overlaps with oesophageal cancer ^[6].

An epigastric mass narrows the differential considerably, but you still need to consider non-gastric causes ^[5][14].

CBP, LFT, RFT are the mandatory baseline investigations ^[5][16].

CEA, CA19-9, CA125 ^[3][16]

Upper endoscopy and biopsies ^[5][16] — this is the single most important investigation. It serves two purposes:

1. Obtain tissue diagnosis (histological confirmation of malignancy)
2. Evaluate extent of primary tumour endoscopically ^[2]

Why OGD is the gold standard:

• Direct visualisation of the gastric mucosa with magnification
• Ability to take multiple targeted biopsies from suspicious lesions
• Assessment of tumour location, size, morphology (Borrmann type), and involvement of the GOJ
• Therapeutic potential (e.g., endoscopic mucosal resection for early gastric cancer)

Endoscopic findings in gastric cancer:

Biopsy technique:

• At least 6–8 biopsies should be taken from the margin of any gastric ulcer (multiple quadrants) to maximise diagnostic sensitivity — a single biopsy has only ~70% sensitivity, but 7 biopsies reaches > 98%
• For suspected linitis plastica: use deep "strip and bite" biopsy technique — standard mucosal biopsies are insufficient because the tumour is submucosal ^[3]
• Biopsies of normal-appearing mucosa in the antrum and body should also be taken to assess for H. pylori, atrophic gastritis, and intestinal metaplasia (the Sydney protocol: 5 biopsies — 2 antrum, 1 incisura, 2 body)

Advanced endoscopic techniques:

• Narrow-band imaging (NBI): Uses specific wavelengths of light to enhance surface mucosal and vascular patterns — helps distinguish neoplastic from non-neoplastic lesions without dye application
• Chromoendoscopy: Application of dyes (e.g., indigo carmine, methylene blue) to enhance mucosal detail — useful for detecting early gastric cancer and defining margins for endoscopic resection
• Magnification endoscopy: Allows detailed assessment of mucosal pit patterns and microvascular architecture

Histological analysis from biopsy should determine:

• Histological type (adenocarcinoma vs lymphoma vs GIST vs other)
• Lauren classification (intestinal vs diffuse)
• Grade of differentiation (well / moderately / poorly differentiated)
• HER2 status (by IHC ± FISH) — essential for treatment decisions (trastuzumab eligibility; HER2 +ve in ~15% of intestinal type) ^[2]
• Microsatellite instability (MSI) / mismatch repair (MMR) status — for immunotherapy eligibility
• PD-L1 combined positive score (CPS) — for checkpoint inhibitor eligibility
• EBV status (EBER ISH)

Alternative to OGD — Barium Swallow/Meal:

• Limited diagnostic value except for linitis plastica ^[2]
• Shows a non-distensible "leather bottle" stomach with loss of mucosal folds — the classic radiographic appearance
• Cannot take biopsies — so even if barium is suggestive, OGD is still needed
• Largely superseded by OGD in modern practice but still useful when OGD cannot adequately assess gastric distensibility

Diagnostic imaging is valuable for: ^[5]

• Staging — chest x-ray, CAT scan, PET scan
• Diagnosis of:
  • Intestinal obstruction
  • Malignant biliary obstruction
  • Malignant ureteric obstruction
• Monitoring response to treatment

From the lecture slides, the clinical staging workup consists of:

• History and physical examination
• Liver function test
• Chest x-ray
• Ultrasonography or CAT scan abdomen
• PET/CT scan
• Endoscopic ultrasound
• Laparoscopy

^[5]

As covered earlier, linitis plastica presents a unique diagnostic problem:

• Mucosa may appear "normal" on endoscopy ^[5]
• Rigid, could not be distended with air ^[5]
• Standard mucosal biopsies → false negatives because the tumour infiltrates the submucosa and muscularis propria ^[3]

Diagnostic approach:

1. Deep strip-and-bite biopsies (grab deeper tissue including submucosa)
2. EUS — shows diffuse hypoechoic wall thickening involving the 3rd and 4th layers (submucosa and muscularis propria)
3. Barium swallow — may be superior to OGD for this specific entity; shows the classic non-distensible stomach with narrowed lumen and loss of rugal folds ^[2]
4. CT — shows diffuse circumferential gastric wall thickening

• HER2 (Human Epidermal growth factor Receptor 2) is a transmembrane tyrosine kinase receptor; when amplified/overexpressed, it drives uncontrolled cell proliferation
• HER2 +ve in ~15% of gastric cancers (predominantly intestinal type) ^[2]
• Testing method: IHC first → if 2+ (equivocal) → confirm with FISH (fluorescence in situ hybridisation)
• A positive HER2 result qualifies the patient for trastuzumab (Herceptin) — a monoclonal antibody targeting HER2 — in combination with chemotherapy

Indications: early gastric CA confined to mucosa (T1a) — diagnosed by endoscopic white light picture (not EUS!) ^[2]

The rationale is based on lymph node metastasis risk:

• T1a (mucosal): LN metastasis risk ~3–5% (acceptable for endoscopic resection if other criteria met)
• T1b (submucosal): LN metastasis risk ~15–25% → requires surgical resection with lymphadenectomy ^[3][17]

Expanded criteria for endoscopic resection (Japanese Gastric Cancer Treatment Guidelines 2021):

^[2][3]

After EMR/ESD, the resected specimen is meticulously assessed histologically:

• Lateral margins — clear or involved?
• Deep margin — clear or involved?
• Depth of invasion — T1a (mucosal) vs T1b (submucosal)?
• Lymphovascular invasion (LVI) — present or absent?
• Differentiation — well/moderately vs poorly differentiated?

Histology determines margin (lateral and deep) — consider curative if clear; salvage gastrectomy if T1b+ ^[2]

If curative criteria are met → endoscopic surveillance annually ^[2] If non-curative (T1b, positive margins, LVI, undifferentiated) → salvage gastrectomy with lymphadenectomy

1. Complete resection with negative microscopic margins (R0 resection) ^[3]

   • Gross negative margins of ≥ 5 cm are required from the macroscopic tumour edge ^[3]
   • Why 5 cm? Because gastric cancer (especially diffuse type) can have microscopic intramural extension beyond the visible tumour margin. A wide margin minimises the risk of positive microscopic margins.
   • Intraoperative frozen section of the proximal resection margin is performed to confirm negative margins in real time

2. Adequate lymphadenectomy — at minimum, D2 (see below)

3. En bloc resection of adjacent involved organs in T4b tumours — e.g., distal pancreas, transverse colon, spleen ^[3]

Tumours are considered unresectable (i.e., curative-intent surgery is not appropriate) if:

• Distant metastasis (e.g., multiple liver metastases, peritoneal nodules, pelvic deposits, Virchow's nodes) ^[17]
• Extensive nodal involvement (D3) ^[17]
• Invasion of major vascular structures: aorta, hepatic artery, coeliac axis, proximal splenic artery ^[3][17]
  • Note: Distal splenic artery involvement = borderline resectable with LUQ exenteration ^[17]
  • Portal vein involvement is NOT an absolute contraindication — venous resection may be considered in selected centres to achieve R0 ^[18]
• Positive peritoneal cytology on staging laparoscopy (= M1) ^[2]

The extent of gastric resection depends on the location of the tumour:

Gastric resection with D2 lymph node dissection ^[5]:

• Distal resection for distal lesion ^[5]
• Total gastrectomy for proximal lesion ^[5]

Common reconstruction patterns after gastrectomy:

Why Roux-en-Y for total gastrectomy?

• After total gastrectomy, the oesophagus is anastomosed to a Roux limb of jejunum (a defunctionalised limb)
• This prevents bile reflux oesophagitis — a major problem with direct oesophagojejunostomy without a Roux limb, because bile and pancreatic juices would reflux into the oesophagus causing severe chemical injury
• Roux-en-Y oesophagojejunostomy is the standard reconstruction ^[5]

This is a critically important concept and frequently examined:

D2 lymphadenectomy is the STANDARD of care in patients with potentially curable gastric cancer ^[3][5]

Why D2 over D1?

• Better disease-specific survival ^[3]
• Allows more accurate N staging — minimises stage migration (Will Rogers phenomenon: removing more LNs → some N0 patients reclassified as N+ → apparent improvement in survival of both groups without any real treatment benefit — D2 avoids this artifact by providing a truer staging picture) ^[3]
• Requires removal of at least 15 lymph nodes for adequate staging (AJCC recommends ≥16) ^[3]

The trade-off:

• Higher perioperative morbidity and mortality compared to D1 — historically related to routine splenectomy and distal pancreatectomy performed during D2, which are now largely avoided unless the spleen/pancreas is directly invaded ^[3]
• In experienced centres (Japan, Korea, Hong Kong), the morbidity of D2 is now comparable to D1

Minimally invasive approach:

• Laparoscopic gastrectomy is increasingly performed for early gastric cancer ^[5] and even for advanced disease in experienced centres
• Benefits: reduced blood loss, shorter hospital stay, less postoperative pain, comparable oncological outcomes (in experienced hands)

Preop neoadjuvant chemotherapy — selected patients ^[5]

HK: Upfront surgery is preferred — only consider if T3+ / N+ ^[17]

Rationale for neoadjuvant chemotherapy:

• Downstage the tumour to improve resectability rate ^[17] — shrink a borderline-resectable tumour to make R0 resection achievable
• Reduce rate of local and distant recurrence ^[3] — by treating micrometastatic disease early, before it becomes clinically apparent
• Allows assessment of in vivo chemosensitivity — if the tumour responds to neoadjuvant therapy, the same regimen can be continued adjuvantly; if it progresses, the regimen can be changed

Indications:

• T3+ (transmural) tumours or N+ (LN involvement) ^[3][17]
• Borderline resectable disease

Regimens:

Postop adjuvant chemotherapy — for advanced cancer ^[5]

Rationale:

• Eradicate micrometastasis remaining after surgery ^[17]
• Reduce risk of local and systemic recurrence

Indications:

• After upfront R0/D2 resection, pathological stage II–III usually warrants adjuvant chemotherapy; stage I and exceptional molecular/risk groups require their own assessment
• Consider if T3+ / N+ ^[17]

Regimens:

These are increasingly integrated into the treatment algorithm:

• Transfusion — for anaemia from chronic GI blood loss
• PPI — reduce acid secretion, promote ulcer healing, reduce bleeding
• Iron supplementation — for iron deficiency anaemia
• Pain control — WHO analgesic ladder; consider coeliac plexus block for intractable epigastric/back pain
• Nutritional support — oral supplements, enteral feeding (NJ tube), parenteral nutrition if necessary

Endoscopic stenting ^[5] — quick, minimally invasive, provides rapid symptom relief, but less durable than surgical bypass.

Palliative resection: relieve bleeding / obstruction ^[17] Palliative bypass (gastrojejunostomy): more durable than stenting, but possible impaired gastric emptying / bile reflux ^[17]

Palliative chemo ± HER2 inhibitor (if HER2 +ve) ± ramucirumab (VEGFR2 antagonist) ^[17]

For patients with metastatic or unresectable gastric cancer who have adequate performance status:

External beam radiotherapy (EBRT) for painful bone metastases ^[17] — highly effective for pain palliation; single-fraction (8 Gy) or multi-fraction (30 Gy in 10 fractions) regimens.

Mechanism: The tumour ulcerates through the gastric mucosa → erosion of submucosal and mucosal blood vessels → bleeding into the GI lumen. This can be:

• Chronic occult bleeding → iron-deficiency anaemia (hypochromic microcytic) ^[19]
  • Why iron deficiency? Chronic slow blood loss depletes iron stores faster than dietary intake can replenish them. Red blood cells cannot be loaded with haemoglobin without iron → microcytic, hypochromic anaemia.
  • Often insidious — the patient gradually becomes fatigued, pale, and short of breath without realising they are bleeding.
• Acute overt bleeding → haematemesis and melaena ^[19]
  • Haematemesis (vomiting blood) occurs when blood accumulates in the stomach; if slow, gastric acid converts haemoglobin to haematin → "coffee-ground" vomitus.
  • Melaena (black, tarry stools) occurs when blood is digested during transit through the GI tract.
  • Massive haemorrhage can present with haemodynamic instability (tachycardia, hypotension, shock).

Management:

• Acute: Resuscitation (IV fluids, blood transfusion), urgent OGD with endoscopic haemostasis (adrenaline injection, clipping, thermal coagulation)
• If endoscopy fails: Transcatheter arterial embolisation (TAE) or palliative surgery ^[17]
• Chronic: Iron supplementation (oral or IV), PPI (reduces acid-mediated re-bleeding), blood transfusion as needed ^[17]
• Palliative resection for bleeding ^[5] — in unresectable disease with refractory bleeding, palliative gastrectomy removes the bleeding source
• External beam radiotherapy (EBRT) can reduce tumour vascularity and control bleeding ^[3][17]

Mechanism: Tumour at the antrum or pylorus progressively narrows the gastric outlet → food cannot pass into the duodenum → proximal gastric distension.

Clinical features:

• Abdominal distension ^[19]
• Vomiting — characteristically non-bilious (obstruction is proximal to the ampulla of Vater), projectile, containing undigested food eaten hours or days previously ^[19]
• Succussion splash (audible splash on shaking the abdomen > 3 hours post-prandially)
• Progressive weight loss and dehydration

Metabolic consequences:

• Risk of dehydration and electrolyte abnormalities including hyponatraemia, hypokalaemia, and metabolic alkalosis ^[19]

  • Why? Repeated vomiting of gastric acid (HCl) → loss of H⁺ and Cl⁻ → hypochloraemic metabolic alkalosis
  • Volume depletion → activation of the renin-angiotensin-aldosterone system → aldosterone promotes Na⁺ reabsorption in exchange for K⁺ and H⁺ excretion in the distal nephron → hypokalaemia + paradoxical aciduria (the kidneys excrete H⁺ to preserve K⁺ and Na⁺, worsening the alkalosis)
  • This is a classic exam concept: vomiting → hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria

• Risk of aspiration pneumonia ^[19] — retained gastric contents can be regurgitated and aspirated into the lungs, especially in debilitated patients or when lying flat

Management:

• "Drip and suck" — NPO, IV fluids (normal saline + KCl), nasogastric decompression ^[12]
• IV PPI to reduce gastric secretion
• Palliative bypass (GJ) for outlet obstruction ^[5] — gastrojejunostomy bypasses the obstructed pylorus
• Endoscopic stenting ^[5] — self-expandable metal stent (SEMS) across the obstructing tumour for rapid relief
• Systemic chemotherapy ^[5] — may shrink the tumour and relieve obstruction
• If resectable: curative gastrectomy addresses both the cancer and the obstruction

Mechanism: Tumour necrosis and ulceration → full-thickness erosion through the gastric wall → loss of wall integrity → gastric contents (acid, food, bacteria) leak into the peritoneal cavity.

Consequence: Leads to peritonitis ^[19]

Clinical features:

• Sudden-onset severe generalised abdominal pain
• Board-like rigidity (involuntary guarding) — generalised peritoneal inflammation causes reflex contraction of the abdominal wall muscles
• Absent bowel sounds (paralytic ileus from peritoneal irritation)
• Sepsis (fever, tachycardia, hypotension)
• CXR: pneumoperitoneum (free gas under the diaphragm — gas escapes from the perforated stomach)

Management:

• Emergency resuscitation (IV fluids, broad-spectrum antibiotics, analgesia)
• Emergency surgery: exploration, washout, and either primary repair with omental patch (if small perforation in a palliative setting) or gastrectomy (if tumour is resectable)
• This is a rare presentation of gastric cancer and carries a poor prognosis

These are not "complications" in the traditional sense but rather the clinical consequences of tumour spread:

These occur due to tumour-secreted substances, not direct invasion: